My training spans pharmaceutical sciences, biomedical research, and postdoctoral work at the intersection of cannabis pharmacology and immunology. As I look toward the next stage of my career, this portfolio highlights the technical versatility, analytical discipline, and translational mindset I hope to bring to collaborative program focused on improving human health.
University of California, Riverside
7/2018 - 9/2023 Riverside, CA
Key Interests
Metabolic dysfunction
Endocannabinoid signaling
Adipoinsular regulation
University of California, Irvine
9/2013 - 6/2017 Irvine, CA
Key Interests
Pharmacokinetics & pharmacodynamics
Lipid nanoparticle drug delivery
GPCR signaling cascades
Postdoctoral Research
HIV-associated neurocognitive disorders remain a major complication for people with HIV, even in the setting of suppressive antiretroviral therapy. Although HIV does not directly infect neurons, persistent viral reservoirs, chronic immune activation, glial dysfunction, and peripheral immune-cell trafficking into the CNS can promote neuroinflammation, mitochondrial stress, synaptodendritic injury, and cognitive impairment.
My postdoctoral work investigates how cannabis exposure and cannabinoid signaling may shape these neuroimmune processes, with a focus on monocyte-derived macrophages, inflammatory signaling, mitochondrial function, and biomarkers linked to cognitive outcomes. This research examines whether cannabis-associated immune phenotypes shift macrophages away from glycolytic, pro-inflammatory states toward more oxidative, anti-inflammatory, and neuroprotective profiles, while recognizing that cannabinoid effects are highly context-dependent and influenced by exposure pattern, inflammatory environment, and disease status.
The therapeutic relevance of this work lies in its potential to support more personalized approaches to neuroimmune health in people with HIV. By identifying how cannabis exposure patterns, inflammatory states, and immune-metabolic profiles interact, this research may help distinguish when cannabinoid-related signaling is protective, neutral, or potentially harmful. These findings could inform biomarker-driven strategies for risk stratification, therapeutic targeting, and individualized interventions aimed at reducing neuroinflammation and preserving cognitive function.
Graduate Research
The endocannabinoid system is a lipid signaling network that regulates appetite, energy balance, inflammation, glucose homeostasis, and communication between metabolic organs. Through endocannabinoids such as 2-AG and anandamide, and receptors including CB1 and CB2, this system links the brain, gut, liver, adipose tissue, and pancreas in pathways that influence feeding behavior, insulin sensitivity, adipokine signaling, hepatic glucose production, and inflammatory tone.
My graduate work focused on how cannabinoid signaling contributes to metabolic dysfunction in diet-induced obesity, with particular interest in the gut-brain axis and the adipoinsular network connecting adipose tissue, pancreatic insulin secretion, and blood glucose regulation. This research investigated how THC and cannabis-derived compounds alter obesity-associated metabolic phenotypes, including body weight, adipose biology, glucose tolerance, insulin-related pathways, and tissue-specific metabolic signaling.
The therapeutic relevance of this work centers on understanding how cannabinoid biology can be leveraged or selectively modulated in metabolic disease. By comparing the effects of isolated THC, cannabis extract, and tissue-specific cannabinoid signaling pathways, this research highlights the importance of compound composition, receptor context, and metabolic state in determining therapeutic outcomes. These findings support a more nuanced, personalized approach to cannabinoid-based interventions, where metabolic phenotype, tissue-specific mechanisms, and disease stage may guide safer and more effective strategies for treating obesity-associated dysfunction.
Office: 858-341-5004
Mobile: 661-202-2539
Copyright 2026 Portfolio by BA
